Langerhans' cells: a distinctive member of bone marrow-derived dendritic cells.
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Animals↗
Biomedical subjects
N Romani
Publications and source records attributed to N Romani.
Effects of physicochemical agents on murine epidermal Langerhans cells and Thy-1-positive dendritic epidermal cells.
The possibility that Thy-1-positive dendritic epidermal cells (Thy-1+DEC) may contribute to the immunologic functions of murine epidermal cells (EC) prompted us to simultaneously assess the effects of certain immunomodulating physicochemical agents on both Thy-1+DEC and Ia-bearing Langerhans cells (LC). C3H/He mice received one of the following treatment modalities: UV-B irradiation (four consecutive days); psoralen plus UV-A (PUVA; three times a week for three consecutive weeks); topically and systemically applied glucocorticosteroids (GCS). Beginning 2 days after the last treatment, animals were sacrificed and the structure and surface marker expression of Ia+EC and Thy-1+DEC were assessed by immunohistologic means on epidermal sheet preparations from ear skin by using appropriate monoclonal antibodies. Whereas low-dose UV-B irradiation (4 X 100 or 200 J/m2) had little, if any, effect on either Ia+EC or Thy-1+DEC, high-dose UV-B (4 X 700 or 1000 J/m2) or PUVA treatment led to an almost complete disappearance of both surface characteristics. Immunoelectron microscopic studies revealed that in the case of LC, high-dose UV-B or PUVA treatment results in the disappearance of their anti-Ia reactivity but leaves their ultrastructural morphology intact. In sharp contrast, Thy-1+DEC escape ultrastructural detection after PUVA treatment and are greatly reduced in number after high-dose UV-B. Ia+EC continuously reappeared with both treatment modalities over a course of 4 to 6 wk, whereas even after 14 to 22 wk Thy-1+DEC were present only in negligible numbers. Similar to high-dose UV-B or PUVA therapy, administration of GCS resulted in the disappearance of both anti-Thy-1- and anti-Ia-reactive cells. Ultrastructural studies disclosed, however, that these steroid-induced alterations in the surface characteristics were accompanied by a dramatic reduction of the LC population but were not paralleled by morphologic changes of Thy-1+DEC. In the course of 7 wk after cessation of steroid treatment, the number of both Ia+EC and Thy-1+DEC had returned to normal values. The selective removal of either of these two dendritic epidermal cell populations by physicochemical agents may provide an excellent strategy to further clarify the functional properties of both LC and Thy-1+DEC.
Animals↗
[Electron microscopy diagnosis of intraocular herpes infection with a case demonstration].
The tentative diagnosis of herpetic anterior uveitis was confirmed by means of an analysis of the aqueous humor employing the electron-microscopic negative contrast method; Acyclovir therapy was subsequently administered. The case is described and routine application of the method is discussed.
Acyclovir↗
Ontogeny of Ia-positive and Thy-1-positive leukocytes of murine epidermis.
Murine epidermis harbors 2 populations of dendritic leukocytes: Langerhans cells (LC) and Thy-1-positive dendritic epidermal cells (Thy-1 +DEC). In the adult mouse these cell types are morphologically distinct and display highly characteristic phenotypes. LC bear Ia-antigens and a group of markers typical for mononuclear phagocytes: Fc- and C3bi-receptors, macrophage-specific antigen F4/80, and membrane ATPase. Thy-1 +DEC, in contrast, lack these markers but express high levels of Thy-1 and asialo-GM1 (asGM1) antigen. Since LC and Thy-1 +DEC share a common origin from the bone marrow we expected to gain insight into their relationship by studying their ontogenetic development. Epidermal sheets from fetal and newborn C3H/He and C57B1/6 mice obtained at defined ages from day 17 of gestation up to day 30 of postnatal life were monitored for the emergence of the above-mentioned markers for LC and Thy-1 +DEC. In double-labeling experiments LC markers were first detected by visualizing the monoclonal antibodies by a sensitive triple-layer rhodamine-immunofluorescence technique; in a second step, after appropriate blocking procedures, Thy-1 and asGM1 antigens were demonstrated by direct and indirect immunofluorescence. We found that in fetal epidermis, only few cells expressed either Thy-1 or Ia (4 and 1 cells/mm2, respectively, on day 18 of gestation). The bulk of Thy-1 +DEC and Ia +EC appeared only after birth. Adult proportions of Thy-1 +DEC and Ia +EC were reached at around 1 month of postnatal life. In contrast, all the other LC markers were expressed on a substantial number of fetal dendritic cells (280 cells/mm2 on day 18 of gestation), indicating the presence of phenotypically immature Ia-negative LC in fetal epidermis. By day 4 of postnatal life all F4/80 +EC and ATPase +EC (i.e., LC) had acquired Ia-antigens. Surprisingly, LC also bore asGM1 antigens, which in the adult epidermis are strictly confined to Thy-1 +DEC, up to day 5 of postnatal life. Thus, LC in fetal and early newborn epidermis are not yet fully differentiated. As they differentiate, they acquire Ia antigens and lose asGM1 antigens. In contrast, a phenotypically immature Thy-1 +DEC population could not be traced with the markers used. Thy-1 +DEC appear to be characterized by a stable phenotype (Thy-1+/asGM1+) throughout their lifetime.
Age Factors↗
Enrichment of murine Langerhans cells by panning with pan-leukocyte monoclonal antibodies.
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Animals↗
Apoptotic keratin bodies as autoantigen causing the production of IgM-anti-keratin intermediate filament autoantibodies.
The presence of numerous keratin bodies in the upper dermis is a characteristic finding in skin lesions of patients with various dermatoses such as cutaneous graft-versus-host disease, lichen planus, or chronic discoid lupus erythematosus. These keratin bodies are generated by apoptotic keratinocyte death, consist largely of keratin intermediate filaments (KIF), and are constantly covered with immunoglobulins, mainly IgM. Apoptosis is also thought to occur under physiologic conditions in the skin as it does in other organs, but keratin bodies are not frequently reported as being found in nonlesional skin. In order to assess the frequency of keratin bodies in normal skin, we examined serial sections of 10 normal human skin specimens and 5 dermal sheets prepared from normal human skin for the presence of keratin bodies. They were visualized by direct immunofluorescence using a fluorescein isothiocyanate (FITC) rabbit antihuman IgM conjugate. In addition the KIF origin of keratin bodies was demonstrated by a double-staining immunofluorescence procedure using a FITC-conjugated rabbit antihuman IgM followed by a mouse monoclonal antibody against keratin and a sheep antimouse immunoglobulin conjugated with Texas Red. One specimen was also examined for keratin bodies at the ultrastructural level. In serial sections, all 10 normal human skin specimens had numerous keratin bodies as assessed by visualization of globular IgM deposits. Evaluated on dermal sheets, the number of keratin bodies ranged from 39-262 per mm2. Nearly all keratin bodies also stained with the antikeratin antibodies. Ultrastructurally the remarkable number of keratin bodies, which consist of filaments measuring approximately 10 nm in diameter or of more granular material, in normal human skin was confirmed. In order to investigate the capacity of KIF material in keratin bodies to function as autoantigen, we examined the sera of the 10 skin donors and, in addition, of 30 normal healthy individuals and 10 patients with rheumatoid arthritis for the occurrence and specificity of IgM-anti-KIF autoantibodies by an enzyme-linked immunosorbent assay and by immunoblot. IgM-anti-KIF autoantibodies were found in all 50 test sera. In the majority of the sera the specificity of these autoantibodies included the 51 kD and the 58 kD KIF protein, which are constituents of KIF in keratin bodies and basal keratinocytes. Quantitatively, the antibody activity of the IgM-anti-KIF autoantibodies varied from serum to serum, being highest in the sera of patients with rheumatoid arthritis.(ABSTRACT TRUNCATED AT 400 WORDS)
Absorption↗
Immediate pigment darkening phenomenon. A reevaluation of its mechanisms.
Proposed mechanisms of immediate pigment darkening (IPD) are controversial. They include photooxidation of "premelanin," changes in the distribution pattern of microfilaments and microtubules, movement of melanosomes to melanocyte dendrites, increased transfer of melanosomes to keratinocytes, and changes in the melanosome distribution pattern in keratinocytes. We investigated the following aspects of IPD: production of IPD by UVA under physiologic and nonphysiologic conditions in fullthickness skin and epidermal sheets; reversibility of IPD in vitro after in vivo and in vitro production; blocking of IPD by disruption of the microfibrillar or microtubular system in vitro; alterations of the cytoskeleton of melanocytes; the melanosome distribution pattern in melanocytes and keratinocytes. The results were as follows: IPD could be elicited in vitro in full-thickness skin and in epidermal sheets. Its production was temperature independent (0 degrees-37 degrees C) and was not inhibited by repeated freezing and thawing, or by formalin fixation. IPD was reversible in vitro under tissue culture conditions but only in viable skin. IPD could not be blocked by substances that disrupt the microfibrillar or microtubular system (cytochalasin B, colcemid, vincristine). As shown with a monoclonal antivimentin antibody, IPD-producing UVA doses did not induce changes in the cytoskeleton of melanocytes. No changes in number and distribution pattern of melanosomes were observed electron-microscopically and by morphometric analysis of EM micrographs. Production of IPD does not depend on the structural and functional integrity of the melanocyte cytoskeletal apparatus and is not confined to viable skin, whereas its reversibility is. The fact that no increased melanosome transfer occurs may explain the lack of a UV protective action.
Cytochalasin B↗
HLA-DR expression on keratinocytes is a common feature of diseased skin.
Biopsy specimens from 185 patients with 52 different skin disorders were investigated by indirect immunofluorescence staining for the presence of HLA-DR bearing keratinocytes and their association with an underlying inflammatory infiltrate and in particular with activated (HLA-DR-positive, Leu-4-positive) T lymphocytes. HLA-DR expression on keratinocytes was demonstrated in 38 dermatoses, including lymphocytic vasculitis, lupus erythematosus, morphea, vitiligo, lichen planus, cutaneous T-cell lymphoma, various infectious dermatoses, allergic contact dermatitis, granulomatous dermatoses, Sweet's syndrome, lichen sclerosus and erythema nodosum. In 27 of these this had not previously been reported. Occurrence of HLA-DR on keratinocytes was invariably linked to the presence of a lymphocytic infiltrate containing numerous activated T-cells (Leu-4 +, HLA-DR +) whereas such infiltrates were not accompanied by HLA-DR expression on keratinocytes in all the dermatoses investigated, as in pseudolymphoma and erythema anulare centrifugum. However, HLA-DR positive keratinocytes were consistently absent in skin disorders lacking any significant lymphocytic infiltration (e.g. leukocytoclastic vasculitis, bullous autoimmune dermatoses, genodermatoses and mastocytosis). Although it has been suggested that HLA-DR-positive keratinocytes are involved in various immune responses of the skin, their exact functional significance is, as yet, unknown.
Epidermis↗
Effects of short-wave UV and PUVA treatment on structure and phenotype of bone marrow-derived dendritic cells of the mouse epidermis.
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Animals↗
The Thy-1-bearing cell of murine epidermis. A distinctive leukocyte perhaps related to natural killer cells.
Bone marrow-derived leukocytes of murine epidermis can express two phenotypes: typical Langerhans cells, which are Ia+ and Thy-1-, and a recently discovered second population that is Thy-1+ and Ia-. To verify that these phenotypes are expressed by two different cell types, and to help understand their lineage and function, we have studied morphology and reactivity with a large panel of antibodies. Dual antibody immunofluorescence combined with electron microscopy showed that Thy-1+ and Ia+ cells were each distributed in a regular fashion and formed adjacent dendritic systems in or close to the basal layer. Double-labeling studies with anti-Ia and a second monoclonal antibody revealed that all Langerhans cells expressed F4/80 (macrophage), Mac-1 (C3bi receptor), and 2.4G2 (Fc receptor), as well as the thymus leukemia (TL) and heat-stable (M1.69/16) antigens. A large fraction expressed S100 and all exhibited membrane ATPase and nonspecific esterase. In contrast, Thy-1+ cells lacked all these features of Langerhans cells, except that a minority were strongly reactive with 2.4G2. Thy-1+ cells also lacked differentiation antigens of most other types of leukocytes, except they were rich in asialo GM1. By electron microscopy, Thy-1+ cells had cytoplasmic granules that were similar in structure and in their aryl sulfatase content to those previously described in natural killer cells. The granules were enlarged in beige mice, suggesting a lysosomal origin, and were present in mast cell-deficient W/Wv mice, indicating no relation to mast cells. We conclude that Thy-1+ epidermal cells are thoroughly distinct from Langerhans cells. On the basis of morphology and phenotype, they may represent a type of tissue natural killer cell. Thy-1+ natural killer cells are now being identified in several nonlymphoid sites, such as gut epithelium and the livers of mice given adjuvants. If Thy-1+ epidermal cells prove to be natural killer cells, it is noteworthy that they represent a resident population regularly distributed in the basal layer of all mouse strains. The notion that Thy-1+ epidermal cells are immature natural killer cells is intriguing in light of recent evidence that Ia+ Langerhans cells are also immature with respect to accessory cell function. The epidermis may not have the functional capacities of a lymphoid organ, but it could contribute immature cells important for both natural and acquired resistance.
Animals↗
Human interferon-gamma induces expression of HLA-DR on keratinocytes and melanocytes.
Primary human epidermal cell cultures composed of keratinocytes and melanocytes were exposed to supernatants of phytohaemagglutinin (PHA)-stimulated T cells, various lymphokines and interferon-beta, and checked for the emergence of HLA-DR antigen using immunofluorescence and immunoelectron microscopy. HLA-DR expression was induced by the supernatants and human recombinant interferon-gamma (rIFN-gamma), whereas recombinant interferon-alpha 2, interleukin-2 and non-recombinant human interferon-beta had no such effect. The threshold concentration of rIFN-gamma required to induce this phenomenon was 10 IU/ml; no further increase of reaction intensity was observed using doses of more than 100 IU/ml. Maximum reaction intensity was achieved after 72 h of incubation; a minimum of 3 h of incubation with rIFN-gamma followed by 72 h incubation in rIFN-gamma-free medium proved sufficient to induce HLA-DR expression. The inductive effect of the supernatants and rIFN-gamma could be completely abrogated by pretreatment with excess doses of the monoclonal antibody GZ4 specific for human IFN-gamma. Keratinocytes and melanocytes reacted in an identical fashion both qualitatively and quantitatively in all experiments. These data indicate that IFN-gamma possesses specific signal functions in the induction of HLA-DR expression on epidermal cells.
Cells, Cultured↗
Expression of the Ly-5 alloantigenic system on epidermal cells.
The expression of Ly-5 alloantigens is confined to hemopoietic cell types and is therefore considered a valuable indicator for the bone marrow derivation of a given cell. The further finding that different hemopoietic cell lineages express different molecular forms of the Ly-5 alloantigens prompted us to investigate (1) whether murine epidermal cells or subpopulations thereof express Ly-5 specificities and if so, (2) whether the expression of particular molecular configurations of Ly-5 antigens would allow us to gain a clue about the derivation of certain epidermal cell populations. When epidermal sheets from BALB/c, C57Bl/6, and C3H/He mice, were exposed to monoclonal anti Ly-5.1 antibody in an indirect immunofluorescence technique, a system of evenly distributed, dendritic cells was visualized. Allelic exclusion of the Ly-5 system was demonstrated by replacing anti-Ly-5.1 antibody by anti-Ly-5.2 reagent and by using epidermal sheets from SJL/J mice. Studies on epidermal cell (EC) suspensions revealed that about 1.6-5.2% of C3H/He EC were Ly-5-reactive and that approximately equal numbers of Ly-5-positive cells bore either Thy-1 or Ia antigens. Electron microscopic studies disclosed two morphologically different Ly-5-positive cell populations, i.e., cells of the Langerhans cell lineage and a recently defined cell system, whose most prominent feature is the expression of the Thy-1 antigen. We have termed these cells dendritic Thy-1+EC (dTHY-1+EC). In order to define the molecular configurations of the Ly-5 alloantigens, EC and spleen cells were internally labeled and--after immunoprecipitation of cell-membrane detergent extracts with anti-Ly-5.1--were analyzed on sodium dodecyl sulfate-polyacrylamide gels. Spleen cells yielded 3 bands with a molecular weight of 180,000, 195,000, and 215,000, respectively, as is characteristic for T lymphocytes, non-T/non-B cells, and B lymphocytes. In contrast, a single 195,000-200,000 dalton band was found in precipitates of both untreated and Langerhans cell-depleted (anti-Ia+C) EC. These data demonstrate the existence and active biosynthesis of the Ly-5 alloantigenic system on certain EC populations, i.e., Langerhans cells and dThy-1+EC, and therefore imply that both cell types originate from a bone marrow-derived precursor. The expression of the same molecular configuration of Ly-5 alloantigens on both LC and dThy-1+EC suggest that these two cell populations do not belong either to the T-cell or to the B-cell lineage and imply an ontogenetic relationship between dThy-1+EC and Ia-positive EC.
Animals↗
Morphological and phenotypical characterization of bone marrow-derived dendritic Thy-1-positive epidermal cells of the mouse.
Increasing evidence exists that the spectrum of dendritic cells within the epidermis is more complex than previously thought. In addition to Langerhans cells, Merkel cells, and melanocytes, the murine epidermis contains a dendritic cell population whose most prominent phenotypic feature is the Thy-1 antigen. These cells are now generally referred to as dendritic Thy-1+ epidermal cells (dThy-1+EC). The ultrastructural features of these cells do not resemble those of other resident epidermal cells (EC). In particular, their cytoplasm contains abundant intermediate-sized filaments of the vimentin type as well as membrane-limited organelles with a central granular core. The bone marrow derivation of dThy-1+EC is now well established: dThy-1+EC carry Ly-5 determinants whose expression is restricted to cells of the hemopoietic differentiation pathway, and studies using Thy-1-disparate radiation bone marrow chimeras have revealed the presence of donor-type Thy-1+ cells within the epidermis; by immunoelectron microscopy, these cells represent dThy-1+EC. dThy-1+EC repopulate the epidermis at a slower rate than Langerhans cells as evidenced by a direct comparison of the repopulation kinetics of both cell systems in radiation bone marrow chimeras, and by experiments studying the emergence of either Ia+- or dThy-1+EC in an epidermis which had been previously depleted of either Langerhans cells (glucocorticosteroids) or of dThy-1+EC (PUVA). The phenotypical features of dThy-1+EC differ from those of thymus-derived lymphocytes, B cells, dendritic cells, and mononuclear phagocytes. The surface marker repertoire of dThy-1+EC (Thy-1, Ly-5, asialo-GM1) resembles certain members of the rather heterogeneous natural killer (NK) cell system but functional studies are needed to ascertain this contention.
Animals↗
A comparison of murine epidermal Langerhans cells with spleen dendritic cells.
To establish if epidermal Langerhans cells (LC) are related to spleen dendritic cells, we have considered the morphology, phenotype, and function of the 2 cell types in culture. Cultured LC could be partially enriched (up to 50%) on the basis of 2 simple physical properties: nonadherence to plastic, and low buoyant density in dense albumin columns. The morphology of cultured LC and spleen dendritic cells were similar. In particular both cell types had many cell processes and/or veils, and cultured LC lost their distinguishing Birbeck granules. Freshly isolated LC exhibited nonspecific esterase and ATPase, as well as the F4/80 (alpha-macrophage) and 2.4G2 (alpha-Fc receptor) antigens. However all these traits were lost in culture, while Ia and Mac-1 antigens persisted. As a result, the cytochemical and antigenic phenotype of LC became similar to spleen dendritic cells. The one exception was that LC lacked the 33D1 dendritic cell antigen. The function of LC at first differed from spleen dendritic cells in that fresh LC were weak stimulators of T cell proliferation in the mixed leukocyte reaction and in sodium periodate-induced mitogenesis. However, stimulatory activity per cell increased at least 30 fold in culture so that by 2-3 days, LC were 3-10 times more potent than dendritic cells. Maturation of LC function was radioresistant and was accompanied by a small increase in cell surface Ia antigens. Although LC have been likened both to lymphoid dendritic cells and to macrophages, our data suggest a different conclusion. LC seem to be dendritic cell precursors and are immunologically immature. Possibly, lymphoid dendritic cells are in general derived from substantial pools of precursors in nonlymphoid tissues, such as epidermal LC.
Animals↗
Distribution of anionic surface sites on human melanocytes and human melanoma cells in culture.
With cationized ferritin (CF) as an ultrastructural marker for anionic cell surface sites, cultured guinea pig melanocytes display a uniquely homogeneous labelling pattern and a striking absence of redistribution of marker material. In the present study, we applied the same technique to normal human melanocytes and melanoma cells. Unfixed primary human mixed epidermal cell cultures displayed CF labelling patterns identical to those in guinea pig epidermal cells: on keratinocytes, CF was found in distinct aggregations which, upon prolonged incubation, clustered and were shed. Melanocytes, in contrast, bound CF to the cell surface as a uniform diffuse monolayer. There were no signs of cluster formation or shedding. Melanoma cell cultures were derived from 10 primary (2 lentigo maligna, 1 lentigo maligna melanoma, 4 superficial spreading melanomas, 2 nodular portions of superficial spreading melanomas, 1 nodular melanoma) and from 7 metastatic melanomas (4 cutaneous, 3 lymph node metastases). The CF labelling patterns encountered were heterogeneous. Three out of 10 primary tumors and 5 out of 7 metastases showed alterations of the normal melanocyte labelling pattern: regions of typical CF distribution were irregularly interrupted by stretches of membrane free of marker. In some areas, CF occurred in small globular aggregates. There was considerable heterogeneity of CF labelling patterns in different clones of a given culture. Altered CF binding patterns in melanoma cells appear to be associated with high metastasizing protential of the cell clones and may thus represent an unfavourable prognostic sign.
Binding Sites↗
Subsets of epidermal Langerhans cells as defined by lectin binding profiles.
In this study we characterize the cell surface glycoconjugate moieties of strain 2 guinea pig epidermal Langerhans cells (LC) in single cell suspension by using a battery of 17 fluorescent lectins. All LC displayed binding sites for concanavalin A, succinylated concanavalin A, Lens culinaris agglutinin, Pisum sativum agglutinin, wheat germ agglutinin, succinylated wheat germ agglutinin, Griffonia simplicifolia agglutinin I, Ricinus communis agglutinin I, Phaseolus vulgaris E agglutinin, and Phaseolus vulgaris L agglutinin, but failed to bind Sophora japonica agglutinin (SJA), Dolichos biflorus agglutinin (DBA), and Ulex europaeus agglutinin I (UEA I). Neuraminidase pretreatment rendered LC reactive for SJA, but not for DBA and UEA I. The binding profiles of certain lectins point to the existence of LC subpopulations in that Griffonia simplicifolia I-B4 isolectin, peanut agglutinin (PNA), Helix pomatia agglutinin, and soybean agglutinin bound to only 80% (range 70-90%) of Ia-positive epidermal cells; binding sites for these lectins on primarily unreactive Ia-positive cells were unmasked when epidermal cells were treated with neuraminidase prior to lectin labeling. Ultrastructural PNA labeling studies revealed that the vast majority of Birbeck granule-containing LC displayed PNA binding sites, whereas indeterminate cells were consistently PNA-negative. Identification of carbohydrate configurations expressed on LC surfaces by lectin binding may provide a clue for the elucidation of the mechanisms of established LC functions and possibly the discovery of as yet unknown properties of this cell type.
Animals↗
Identical lectin binding patterns of human melanocytes and melanoma cells in vitro.
Cell surface glycoconjugate patterns of human epidermal cells and of melanoma cells (MC) in primary culture derived from 11 primary and metastatic melanomas were investigated using fluorescent and horseradish peroxidase conjugated lectins for visualization at the light and electron microscopic level. The lectin labeling profiles of human melanocytes (M) and MC were found to be identical. According to their binding patterns, the lectins tested were grouped into three categories: (1) lectins binding to both keratinocytes (K) and M/MC, irrespective of neuraminidase pretreatment (concanavalin-A, wheatgerm agglutinin, succinylated wheatgerm agglutinin); (2) lectins binding to K but not to M/MC, irrespective of neuraminidase pretreatment (Ulex europaeus agglutinin I); (3) lectins binding to K, but to M/MC only after neuraminidase pretreatment (soybean, Helix pomatia, and peanut agglutinins). Untreated M were reactive for soybean and peanut agglutinins only at contact sites with K. Since the lectins from soybean, Helix, and peanut bind specifically to D-galactose and N-acetyl-D-galactosamine residues, we conclude that these particular glycoconjugates are normally masked by sialic acid on M/MC surfaces and can be unmasked by neuraminidase. These features, which have been previously observed in guinea pig M, appear to be interspecies surface markers of melanocytic cells which remain unaltered in the course of malignant transformation.
Animals↗
Coated Langerhans cell granules in histiocytosis X cells.
Histiocytosis X cells (HXC) and epidermal Langerhans cells (LC) are thought to be closely related because they share morphologic features and immunologic markers. One of these common markers, the LC granule, is an acknowledged morphologic criterion for the identification of these cell types, but its function and, thus, significance are as yet unknown. In this study, we report the presence of a fuzzy coat radiating from the cytoplasmic face of the LC granule membrane in HXC. This bristly coat is indistinguishable from that of coated vesicles and pits and, thus, represents a strong morphologic clue to the function of LC granules because coated structures have been shown to be involved in the selective transport of molecules in eukaryotic cells.
Adult↗